Though respiratory regulation in newborns has many similarities with adults, quantitative and qualitative differences exist. It is possible that these developmental differences account for the pronounced susceptibility of newborn infants to develop prolonged spontaneous apneic episodes. The present studies are based on the hypothesis that central neural mechanisms are more important in respiratory regulation than traditionally recognized. The principle objective of the study is to develop an understanding of neural mechanisms which inhibit respiratory output and to characterize the influence of these mechanisms on reinitiation of breathing following onset of apnea. An experimental animal model has been developed which eliminates the effect of negative chemical feedback which usually follows a change in ventilation but which allows quantitation of respiratory output by measuring phrenic nerve activity. Newborn piglets are breathed by means of a servo-controlled mechanical ventilator to keep end-tidal PCO2 constant. Stimulation of the superior laryngeal nerve (SLN) is used to induce central apnea. Observations of phrenic nerve activity during and after SLN stimulation allows characterization of the respiratory inhibitory process. This process may involve afterdischarge or reverberation within central neural circuits which serves to deepen and prolong the inhibitory effect of SLN stimulation. Preliminary evidence suggests that naloxone may modify the inhibitory effect of SLN stimulation. This finding implicates endorphins--endogenous opiate-like polypeptide neurotransmitters--as inhibitory modulators of respiratory output. These central inhibitory neural process may have bearing on prolonged apnea spells observed in premature infants and infants at risk for sudden-infant-death syndrome.